Journal of Oral Pathology & Medicine最新文献

Objective: To analyze the expression of B-cell-specific Moloney murine leukemia virus insertion site 1 (BMI1) and mitogen-activated protein kinase 3 (ERK3) in the serum of oral squamous cell carcinoma (OSCC) patients and their relationship with tissue differentiation and lymph node metastasis.

Methods: A total of 200 patients with OSCC from July 2019 to October 2021 were selected as the OSCC group. And 100 healthy physical examination subjects during the same period were selected as the control group according to the 2:1 ratio principle. Serum BMI1 and ERK3 mRNA expression levels were compared between the two groups and across different clinicopathological characteristics in OSCC patients. Their correlations with pathological features were also examined. The expression levels of BMI1 and ERK3 mRNA in the serum of patients with different prognoses in the OSCC group were compared. The prognosis and survival of patients were compared based on different serum levels of BMI1 and ERK3.

Results: The expression levels of serum BMI1 mRNA and ERK3 mRNA in the OSCC group were higher than those in the control group (p < 0.05). There were significant differences in the expression levels of serum BMI1 mRNA and ERK3 mRNA in patients with different degrees of differentiation, lymph node metastasis, and TNM staging (p < 0.05). The expression levels of serum BMI1 mRNA and ERK3 mRNA were negatively correlated with histological grading and positively correlated with lymph node metastasis and TNM staging (p < 0.05). The expression levels of serum BMI1 mRNA and ERK3 mRNA in surviving patients were lower than those in deceased patients (p < 0.05). Before and after adjusting for lymph node metastasis, TNM staging, and other factors, serum levels of BMI1 mRNA and ERK3 mRNA were still the influencing factors of OSCC prognosis (p < 0.05). The survival rate was significantly lower in the high-expression groups than in the low-expression groups (36.2% vs. 81.3% for BMI1, 39.2% vs. 79.7% for ERK3, p < 0.05 for both).

Conclusion: The expression levels of serum BMI1 mRNA and ERK3 mRNA in OSCC patients are increased, which is closely related to the pathological characteristics and prognosis of patients. BMI1 and ERK3 are helpful in evaluating the prognosis of OSCC patients.

Objective: Given that the oral ecological environment undergoes alterations during the pathological progression of type 1 diabetes mellitus (T1DM) with xerostomia, this study employed microbiomics in conjunction with metabolomics to identify the distinct oral microbiota and salivary metabolites in patients with type 1 diabetic xerostomia and healthy individuals, aiming to elucidate the microorganisms, metabolites, and metabolic pathways potentially implicated in T1DM-associated xerostomia.

Methods: Saliva samples were obtained from individuals diagnosed with T1DM and xerostomia (patient group, n = 9) as well as from healthy volunteers (control group, n = 9), and were subsequently subjected to microbiota profiling and untargeted metabolomic analysis. Bioinformatics methodologies were applied to assess the microbiota and metabolomics datasets both independently and integratively.

Results: A total of 88 differential metabolites were identified between the patient and control groups. These metabolites were predominantly enriched in the caffeine and Vitamin B6 metabolic pathways. Additionally, an average of 280 operational taxonomic units (OTUs) were detected, with species diversity found to be lower in the patient group compared to the controls. At the genus level, 20 significantly altered microbial taxa were identified. Differential genera, including Leptotrichia and Corynebacterium, exhibited higher abundance in the patient group, whereas genera such as Haemophilus and Streptococcus were predominantly present in the control group. Correlation analysis indicated that the differential microbiota did not exhibit strong associations with the identified differential metabolites. However, certain oral microorganisms were associated with specific metabolites enriched in the caffeine metabolic pathway.

Conclusion: In summary, the findings demonstrated notable differences in both oral microbiota composition and salivary metabolite profiles between T1DM patients with xerostomia and healthy individuals. Furthermore, a moderate degree of association between the oral microbiome and metabolome was observed, which may serve as a potential biomarker for T1DM-related xerostomia and contribute to the development of targeted therapeutic strategies.

Background: Given the rarity and aggressive nature of osteosarcomas (OS) in the oral and maxillofacial region, understanding their molecular alterations is essential to improve diagnosis, prognosis, and guide targeted therapies. This study aimed to map molecular alterations associated with oral and maxillofacial OS, providing an overview of the genetic mechanisms involved in their development and progression.

Methods: A scoping review was performed following the PRISMA-ScR guidelines. Studies included observational research, case reports, and systematic reviews focusing on molecular alterations in oral and maxillofacial OS. A comprehensive search was conducted across four databases, and findings were synthesized and categorized by molecular characteristics.

Results: A total of 20 studies involving 68 maxillofacial OS cases were included. The average patient age was 39.4 years, with a slight male predominance. The mandible was the most commonly affected site, and chondroblastic OS was the most frequent histological subtype. Genetic alterations were predominantly observed in the TP53 gene, along with alterations in MDM2, CDK4, and other genes. Treatment primarily involved surgery, with or without chemotherapy. Local recurrence occurred in 11.1% of cases, and distant metastases in 16%. At the final follow-up, 69.7% of patients were alive.

Conclusion: This study emphasizes the value of molecular techniques in improving the diagnosis and management of maxillofacial OS. However, further research is needed to fully understand the molecular complexity and optimize therapeutic strategies.

Background: Oral lichen planus (OLP) is highlighted as a chronic inflammatory disease of the oral cavity with an unclear etiopathogenesis. It is also categorized as an oral potentially malignant disorder. This disease is primarily driven by T-cell-mediated immune responses, leading to keratinocyte apoptosis and persistent inflammation. Despite the availability of therapeutic options, including corticosteroids and immunosuppressants, treatment remains challenging due to variable patient responses and disease chronicity. In vitro models play a crucial role in OLP research by mimicking the local inflammatory environment and providing insights into disease mechanisms and potential therapeutic strategies. While traditional two-dimensional (2D) cultures have contributed to the understanding of OLP pathogenesis, they lack the complexity needed to mimic the disease. Recent advancements in three-dimensional (3D) culture approaches, such as organotypic cultures, organ-on-a-chip devices, and microphysiological systems (MPS), offer enhanced physiological relevance by better mimicking immune-epithelial interactions and cytokine responses. However, no standardized in vitro model currently exists that fully recapitulates OLP's chronic inflammatory features and multifactorial pathology.

Methods and findings: This review addresses this critical gap by evaluating existing in vitro models, establishing validation criteria for developing reliable disease models, and identifying key challenges, including the absence of a fully functional immune system, lack of salivary immune components, and difficulties in maintaining stable long-term cultures. By synthesizing current evidence and limitations, we provide a framework for advancing bioengineered platforms and personalized medicine approaches to develop effective, patient-specific therapies for OLP.

Introduction: Oral melanocytic neoplasms, such as oral melanocytic nevi (OMN), oral dysplastic nevi (ODN), atypical melanocytic proliferation (AMP), and oral mucosal melanoma (OMM), represent < 1% of oral lesions. They are composed of pigment-producing cells with distinct biological behaviors. This study aimed to summarize the clinicopathological and molecular features of these lesions.

Methods: Studies published in English (1950-2025) were retrieved from the PubMed database and Web of Science Core Collection. All articles presenting clinicopathological and molecular outcomes of OMN, ODN, AMP, and OMM were included. A narrative summary was created to describe the findings.

Results: OMN and OMM are well-described from a clinicopathological perspective. However, ODN and AMP remain scarcely documented. The genetic landscape of OMN suggests a limited role for driver mutations in BRAF or GNAQ, which promote the proliferation of pigmented-producing cells, often insufficient for malignancy. OMM exhibits a distinct molecular profile characterized by a scarcity of MAPK mutations and numerous copy-number changes, as well as amplifications and chromosomal rearrangements. In contrast, no genetic data are available for ODN and AMP.

Conclusions: Oral melanocytic neoplasms are rare and have distinct clinicopathological features. Despite this, a gap exists in molecular data regarding ODN and AMP. Conversely, OMN and OMM have distinct profiles; in particular, the latter may benefit modestly from tyrosine kinase inhibitor treatment, as KIT and BRAF mutations are sensitive to imatinib and vemurafenib, respectively.

Objectives: Direct immunofluorescence (DIF) is the gold standard for diagnosing subepidermal blistering diseases (SBDs). However, DIF requires specialized expertise; therefore, alternative immunological methods such as enzyme-linked immunosorbent assays (ELISA) are worth exploring. The aim of this review was to evaluate the diagnostic agreement between DIF and ELISA for the diagnosis of SBD.

Materials and methods: A systematic literature review of international journals and electronic databases (MEDLINE via OVID, Scopus, and Web of Science) was conducted between their inception and December 2023. The risk of bias and overall quality of evidence were assessed using the Newcastle-Ottawa Scale and the GRADE system.

Results: Of the 1691 articles identified, 38 were included in the qualitative synthesis and 37 in the quantitative analysis. Three meta-analyses were developed and revealed the superiority of DIF over ELISA, with the following risk differences: BP180, 0.26 (95% CI: 0.19-0.33, p < 0.00001, I²: 96%); BP230, 0.59 (95% CI: 0.47-0.71, p < 0.00001, I²: 98%); and Lam332, 0.82 (95% CI: 0.70-0.94, p < 0.00001, I²: 89%).

Conclusions: DIF remains the gold standard for the diagnosis of autoimmune SBDs. ELISA can serve as a complementary diagnostic tool, especially as a follow-up instrument for patients with SBD, owing to its low invasiveness.

Background: Oral squamous cell carcinoma (OSCC) is one of the most common subtypes of head and neck squamous cell carcinoma (HNSCC), characterized by high recurrence rates and poor prognosis. SPOCD1 has been identified as a facilitator of tumor progression in several cancers; however, its regulatory role in OSCC has not yet been reported.

Design: Using The Cancer Genome Atlas (TCGA) database, we examined SPOCD1 expression in HNSCC tissues. mRNA and protein levels of SPOCD1 in OSCC cells were assessed by RT-qPCR and western blotting. The effects of SPOCD1 on cell proliferation, invasion, and migration were evaluated using CCK-8, colony formation, wound healing, and Transwell assays. Western blotting was performed to confirm the impact of SPOCD1 on the PI3K/Akt/mTOR pathway. The influence of SPOCD1 on tumor growth was further investigated in vivo.

Results: Analysis of the TCGA database revealed that SPOCD1 expression was upregulated in HNSCC tissues, consistent with our experimental data showing increased SPOCD1 expression in OSCC cells. Inhibition of SPOCD1 suppressed cell proliferation, while its overexpression enhanced proliferation. Similarly, SPOCD1 knockdown reduced migration and invasion, whereas overexpression promoted these processes. In addition, SPOCD1 was found to activate the PI3K/Akt/mTOR pathway. In vivo experiments further demonstrated that SPOCD1 significantly accelerated tumor growth.

Conclusion: This study demonstrates that SPOCD1 promotes OSCC growth and metastasis by activating the PI3K/Akt/mTOR pathway, indicating that SPOCD1 may represent a potential therapeutic target for OSCC treatment.

Background: Although studies have demonstrated a relationship between pathogenic microorganisms and oral cancer, no study has demonstrated a relationship between changes in bacterial flora and oral squamous cell carcinoma (OSCC). Therefore, we investigated the association between oral microbiota and oral squamous cell carcinoma using metagenomic analysis.

Methods: Saliva samples from 64 patients with OSCC and 50 healthy controls who visited the Department of Oral Surgery, Tohoku University Hospital, were collected, and bacterial genomic DNA was extracted using polymerase chain reaction amplification. Single-end sequencing was performed using the Illumina MiSeq platform, and sequence data were analyzed using the Quantitative Insights Into Microbial Ecology 2 platform. The Steel-Dwass test was used for between-group comparisons, and Analysis of Compositions of Microbiomes with Bias Correction was used to detect significant differences in microbiome composition.

Results: Significant differences were observed in alpha-diversity indices of bacterial flora (richness, Faith- phylogenetic diversity, Shannon index) in the OSCC group compared to those in the control group. Among the OSCC group, patients with larger tumor diameters and lymph node metastases (T3/T4, N1 or greater) formed independent clusters in the beta diversity analysis of the bacterial flora. Bacteria of the Actinomycetia phylum, such as Actinomyces and Rothia, were significantly reduced in patients with higher stage and pathological grade. Conversely, bacteria of the phylum Spirochaetia and Proteobacteria, particularly those of the genus Treponema, were significantly elevated in advanced cancer cases.

Conclusions: Our results suggest that changes in the oral microbiota may play a role in OSCC development and progression.

Background: Cystadenoma of the salivary glands (CSG) is a rare benign, multicystic neoplasm, representing approximately 1%-4.7% of all benign salivary gland tumors. This study aimed to systematically review the clinicopathological data reported on case reports and case series of CSG.

Methods: This study was conducted in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses statement. Comprehensive searches were performed across PubMed, Web of Science, Scopus, and Embase electronic databases.

Results: A total of 81 studies were included, encompassing 126 cases of CSG. A slight female predominance was observed (54.91%), with a mean patient age of 54.2 ± 21.5 years. The median lesion size was 1.4 ± 1.6 cm. The parotid gland was the most affected site (23.47%). Most cases were asymptomatic (86.58%), and nodular presentation was noted in 70.96%. Mucocele was the most suspected clinical diagnosis. Histopathologically, the papillary subtype was predominant (67.03%), with oncocytic cells prevailing, followed by columnar and cuboidal cell types. Of the 57 cases with available data on growth pattern, 38 were multicystic and 19 unicystic. Immunohistochemical analysis frequently involved the use of p63, MUC4, MUC1, and CK7. All cases were managed surgically, with a recurrence rate of 6.25%. The median follow-up period was 12.1 ± 23.2 months.

Conclusion: CSG is a rare benign tumor that predominantly affects the parotid gland in female patients, typically presenting as a multicystic lesion. Surgical excision remains the treatment of choice, with a generally favorable prognosis.

Background: Autophagy and tumor necrosis factor-alpha (TNF-α) are pivotal in the progression of oral squamous cell carcinoma (OSCC), yet their interplay remains inadequately understood. This study aims to evaluate the interaction between autophagy and TNF-α for OSCC progression.

Methods: Cytokine levels were measured with the Bio-plex assay; autophagy activation was visualized by confocal microscopy. NF-κB p65 activity was assessed via reporter assay, and cell growth was evaluated using CellTiter-Glo, clonogenic assay, and flow cytometry. Clinical data were analyzed using SPSS.

Results: The level of TNF-α decreased in OSCC cells treated with an autophagy inhibitor but increased in OSCC cells under starvation as an autophagy-inducing condition. The production of TNF-α was also lower in OSCC cells knocked down with siULK1 plus siBECN1 or siATG5 plus siATG7 when compared with OSCC cells knocked down with scrambled siRNA under starvation conditions. The addition of TNF-α increased levels of autophagosome and autolysosome in OSCC cells-TNF-α induced expressions of LC3 and P62 by activating RelA. OSCC cells exposed to TNF-α exhibited increased cell viability and autophagy inhibitors reversed the increased cell viability and growth. TNF-α levels were higher in the serum of OSCC patients than in those with precancerous conditions. Elevated levels of TNF-α were linked to poorer disease-specific survival in OSCC patients. The expression of RelA showed a positive correlation with the expression of LC3 and PP62 in OSCC patients. The increased co-expression of TNF-α/P62, TNF-α/LC3, and TNF-α/RelA/PP62 was associated with shorter disease-free survival in OSCC patients.

Conclusion: The reciprocal regulation between TNF-α and autophagy may contribute to tumor progression in OSCC.